The small noncoding DsrA RNA is an acid resistance regulator in Escherichia coli

The small noncoding DsrA RNA is an acid resistance regulator in Escherichia coli
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DOI:
10.1128/jb.186.18.6179-6185.2004
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发表时间:
2004-09-01
影响因子:
3.2
通讯作者:
Belfort, M
Belfort, M
中科院分区:
生物学3区
文献类型:
--
作者:
Lease, RA;Smith, D;Belfort, M

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DSRA RNA是大肠杆菌的一种小的(87个核苷酸)调节性RNA,通过RNA-RNA相互作用来控制特定mRNAs的翻译和周转。DSRA调控的两个靶点是rpos,稳定期和应激反应的sigma因子(S)和H-NS,组蛋白样核蛋白和全球转录抑制因子。受rpos和H-NS全球调控的基因包括应激反应蛋白和致病性大肠杆菌的毒力因子。在这里,通过使用DNA阵列的转录图谱,我们已经识别了DSRA诱导的基因。随着DSRA的过量生产,许多基因的mRNAs的稳态水平增加,包括大肠杆菌的多个耐酸基因。定量引物延伸分析证实了hdeAB、gadAX和gadBC操纵子中单个抗酸基因的诱导。在DSRA突变体中,大肠杆菌K-12菌株和致病性大肠杆菌O157:H7表现出耐酸性折衷。相反,从质粒中过量生产DSRA使酸敏感的DSRA突变体具有极强的耐酸性。因此,DSRA RNA在耐酸性中起着调节作用。DSRA是直接通过碱基配对还是通过rpos和/或H-NS的干扰间接靶向抗酸基因尚不清楚,但无论哪种情况,我们的结果都表明DSRA RNA可能增强致病性大肠杆菌的毒力。
DsrA RNA is a small (87-nucleotide) regulatory RNA of Escherichia coli that acts by RNA-RNA interactions to control translation and turnover of specific mRNAs. Two targets of DsrA regulation are RpoS, the stationary-phase and stress response sigma factor (sigma(s)), and H-NS, a histone-like nucleoid protein and global transcription repressor. Genes regulated globally by RpoS and H-NS include stress response proteins and virulence factors for pathogenic E. coli. Here, by using transcription profiling via DNA arrays, we have identified genes induced by DsrA. Steady-state levels of mRNAs from many genes increased with DsrA overproduction, including multiple acid resistance genes of E. coli. Quantitative primer extension analysis verified the induction of individual acid resistance genes in the hdeAB, gadAX, and gadBC operons. E. coli K-12 strains, as well as pathogenic E. coli O157:H7, exhibited compromised acid resistance in dsrA mutants. Conversely, overproduction of DsrA from a plasmid rendered the acid-sensitive dsrA mutant extremely acid resistant. Thus, DsrA RNA plays a regulatory role in acid resistance. Whether DsrA targets acid resistance genes directly by base pairing or indirectly via perturbation of RpoS and/or H-NS is not known, but in either event, our results suggest that DsrA RNA may enhance the virulence of pathogenic E. coli.